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Deaths Due to Asphyxiant Gases
Published in Sudhir K. Gupta, Forensic Pathology of Asphyxial Deaths, 2022
Thiosulfate reversibly combines with cyanide and with the help of rhodanese it get converted into a less toxic thiocyanate which got excreted in urine. The primary concerns in this administration of the cyanide antidote kit are, it's side effects, which include severe hypotension, methemoglobinemia and hypersensitivity reactions. However, the antidote for methemoglobinemia is methylene blue and this agent will counteract excess methemoglobin formation.
Dermatitis herpetiformis
Published in Lionel Fry, Atlas of Bullous Diseases, 2020
Methemoglobinemia is another common side-effect of dapsone, and presents as cyanosis. The degree of cyanosis is not directly related to the dose of dapsone. The importance of methemoglobinemia is that it will reduce the oxygen-carrying capacity of the blood. Unless severe, methemoglobinemia is not a problem in the young and middle-aged, but in the elderly there may be impaired cardiac and/or cerebral blood flow, which does not cause symptoms but may if the oxygen-carrying capacity of the blood is reduced.
Myeloproliferative Disorders
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Methemoglobinemia is a disorder characterized by the presence of heme iron in the oxidized or trivalent state so that the Hb molecule is incapable of combining with oxygen. It can be an acquired or an inherited disorder.
Rising incidence and high mortality in intentional sodium nitrite exposures reported to US poison centers
Published in Clinical Toxicology, 2021
Sean D. McCann, Marit S. Tweet, Michael S. Wahl
Sodium nitrite is a highly water-soluble salt commonly used in industrial chemistry, pharmaceutical production, food processing, and as a therapeutic agent in the treatment of cyanide poisoning [1,2]. The reported lethal dose of ingested nitrite salts in humans is highly variable with a broad range reported between 0.7 and 6 g of nitrite component [3]. Nitrites and nitrates are strong oxidizing agents that, when ingested, can lead to profound and potentially fatal methemoglobinemia [4]. Most cases of acquired methemoglobinemia are mild and morbidity and mortality are rare outcomes [5]. However, in severe cases, the resulting impaired oxygen delivery to tissues can lead to significant end organ damage. The clinical manifestations of impaired hemoglobin function can be further compounded by underlying medical conditions that may affect blood oxygenation and oxygen delivery to tissues, such as anemia, cardiac disease, and pulmonary pathology [4]. Presenting symptoms can include cyanosis, decreased oxygen saturation, hypotension, and central nervous system (CNS) depression, among many others. Methylene blue, while also an oxidizing agent, is used to treat xenobiotic induced methemoglobinemia. Methylene blue is reduced to leukomethylene blue, which then reduces methemoglobin to hemoglobin [4,6]. Early recognition of sodium nitrite associated methemoglobinemia and prompt treatment with methylene blue is important when caring for these patients in the emergency department.
Fatal Sodium Nitrite Poisoning: Key Considerations for Prehospital Providers
Published in Prehospital Emergency Care, 2021
Matthew R. Neth, Jennifer S. Love, B. Zane Horowitz, Michael D. Shertz, Ritu Sahni, Mohamud R. Daya
Methylene blue (methylthioninium chloride) is the treatment of choice for symptomatic methemoglobinemia. It works by accelerating the enzymatic reduction of ferric (Fe3+) iron to the ferrous (Fe2+) state through its metabolic product leukomethylene blue, ultimately converting methemoglobin to hemoglobin (41,42). The usual dose of methylene blue is 1 to 2 mg/kg of a 1% solution IV administered over five minutes (41). The dose can be repeated in 30 to 60 minutes if the patient is still symptomatic or methemoglobin levels are greater than 30% (41). The maximum total dose of methylene blue is 7 mg/kg, in most situations, but more may be needed in severe cases. There is the possibility that oxidation back to methemoglobin will reoccur at higher doses of methylene blue (41). Methylene blue is ineffective in patients with G6PD deficiency, NADPH methemoglobin reductase deficiency, sulfhemoglobinemia, and hemoglobin M disease (41,42). Recent evidence suggests that methylene blue may also inhibit the downstream effect of nitric oxide and may assist in the treatment of refractory distributive shock (43).
Cyanosis, hemolysis, decreased HbA1c and abnormal co-oximetry in a patient with hemoglobin M Saskatoon [HBB:c.190C > T p.His64Tyr]
Published in Hematology, 2021
Eva-Leonne Göttgens, Kristian Baks, Cornelis L. Harteveld, Kristel Goossens, Adriaan J. van Gammeren
Methemoglobinemia may arise as a result of genetic or acquired causes. Acquired methemoglobinemia is most prevalent and commonly caused by oxidative stress, which can have exogenous or endogenous origins. Endogenous forms of oxidative stress include but are not limited to free radicals such as nitric oxide, hydrogen peroxide and hydroxyl radicals. Exogenous substances may also trigger the oxidation of hemoglobin and this occurs most often as a result of medication. Dapsone, topical anesthetics (benzocaine, lidocaine), anti-malarial agents (chloroquine, hydroxychloroquine) and street drugs account for the majority of iatrogenic methemoglobinemia [25,26]. In addition to the formation of methemoglobin in healthy patients, these drugs may seriously exacerbate the condition of patients who are prone to methemoglobinemia due to genetic mutations causing hemoglobinopathies. Genetic defects that result in methemoglobinemia are commonly found in the CYB5R3 gene, which encodes the cytochrome b5 reductase enzyme. This enzyme is responsible for the reduction of the Fe3+ ion in methemoglobin to Fe2+. Mutations in this gene can both affect the enzymatic stability as well as its catalytic activity [27,28]. Most other genetic defects giving rise to (unstable) methemoglobinemia are hemoglobinopathies that result in the formation of HbM variants due to the defects in the alpha, beta, or gamma globins [29].